Implantable medical devices, such as pacemakers, defibrillators, and cardioverters (which may collectively be referred to herein as implantable cardiac stimulation devices), are designed to monitor and stimulate the heart of a patient that suffers from a cardiac arrhythmia. Using leads connected to a patient's heart, these devices typically stimulate the cardiac muscles by delivering electrical pulses in response to measured cardiac events that are indicative of a cardiac arrhythmia. Properly administered therapeutic electrical pulses may successfully reestablish or maintain the heart's regular rhythm.
In a healthy heart, contractions occur first in the muscles associated with the atrial chambers of the heart, followed by contractions in the muscles associated with the larger ventricular chambers of the heart. In this way, the atria assist in the filling of the ventricular chambers with blood returning from the veins. This increases the end-diastolic volume thereby increasing the stroke volume to enable the ventricles to more efficiently pump blood to the arteries.
Given the interaction of these chambers, efficient operation of the heart is predicated on each of the chambers operating in a proper timing sequence and having contractions that pump a sufficient amount of blood from the chamber. For example, during contraction the right atrium should pump enough blood to optimally “fill” the right ventricle chamber. Moreover, this should occur immediately before the right ventricle begins to contract. In this way, the heart may efficiently pump blood on a repetitive basis.
A healthy heart repetitively contracts in the above described manner in response to the generation and conduction of electrical signals in the heart. These electrical signals are generated in and conducted through the heart during every beat of the heart. A simplified example of these cardiac signals follows.
Activity for a given beat begins with the generation of a signal in a sinus node of the heart. This signal causes contraction to begin first in the atria. The signal from the sinus node propagates via a conduction system to an atrioventricular (“A-V”) node. The signal is inherently delayed for a short period of time (usually less than 200 ms) within the AV node allowing the atria to contract to help to fill the ventricles. The signal then propagates from the A-V node through the bundle of His to the left and right ventricles via a specialized conduction system. Contraction in each ventricle commences in a coordinated manner when the signal “reaches” the respective muscle fibers in the ventricle.
In an attempt to maintain regular contractions in an unhealthy heart a typical stimulation device may track the type and timing of the signals generated by the heart. In this way the stimulation device may determine whether cardiac events (e.g., contractions) are occurring and whether they are occurring at the proper times. In the event contractions are not occurring or are occurring at undesirable times, the stimulation device may deliver electrical pulses to one or more of the chambers of the heart in an attempt to initiate the desired contractions at the desired times.
A typical stimulation device may track cardiac signals through the use of leads that are implanted in one or more of the chambers of the heart. Through the use of amplification, threshold detection and filtering, signals received via the leads may be associated with the cardiac events discussed above. Conventionally, these cardiac events may be referred to as P-waves, R-waves, T-waves, etc. Here, a P-wave corresponds to a contraction (depolarization) of an atrium. An R-wave corresponds to a contraction (depolarization) of a ventricle. A T-wave corresponds to a return to a resting state (repolarization) of a ventricle.
Conventionally, these events have been sensed and characterized in real-time. For example, implantable devices which detect the cardiac rhythm, e.g., spontaneous atrial contractions (or P-waves) and spontaneous ventricular contractions (or R-waves with or without a preceding atrial event), generally utilize the same basic structure for this function: 1) a sense amplifier feeding a threshold detector for cardiac event detection; 2) a refractory period followed by an alert period to qualify the output of the threshold detector; 3) a trigger signal out of the threshold detector during the alert period identifies a P-wave or R-wave; and 4) no trigger signal out of the threshold detector during the alert period results in a pacing pulse at the end of the alert period.
The sense amplifier may include or be associated with a signal filter. Here, a bandwidth of the filter may be selected to allow the signals that the system is attempting to detect to pass through the filter. Ideally, the filter will reject any other signals. That is, these other signals may not pass through the filter or may be significantly attenuated by the filter.
Any signals that pass through the filter may then be provided to the threshold detector. The threshold detector will generate an output signal in the event the amplitude of the signal exceeds a predefined threshold level. The output signal is thus taken as an indication that a certain cardiac event (e.g., an atrial or a ventricular contraction) has occurred.
By analyzing the type and timing of these indications the stimulation device may determine whether stimulation pulses need to be generated. Thus, if the stimulation device detects cardiac events at the appropriate relative times, the stimulation device may simply continue monitoring the received indications. On the other hand, if an indication has not been received for a predefined period of time, the stimulation device may deliver an appropriate stimulation (e.g., pacing) pulse to the heart.
Immediately after pacing or sensing, a blanking period (or refractory period) may be used to block the threshold detector output, preventing redetection of the event or detection of the depolarization created by the pacing pulse. Typically, the latter part of this refractory period includes a type of noise detection which acts to extend the blanking until the input signal has been quiet for some minimal time interval.
At the end of the blanking/refractory period the alert period begins. During the alert period, any signal that exceeds a programmed detection threshold (e.g., a second input to the threshold detector) causes a signal or interrupt to the stimulation device thereby signaling a detection of a cardiac event.
In practice, the above techniques may not always provide a proper indication of cardiac events. For example, very little information about the true nature of a detected event may be available at the point of detection of the typical P-wave or R-wave since the detection may occur close to the leading edge of the event. Moreover, P-wave detection is dependent on the bandpass characteristics of the sense amplifier and the timing of the alert period. As a result, a P-wave detection may identify a true P-wave in some instances and, in other instances, may identify a far-field R-wave, a far-field T-wave, extracardiac physiologic noise or external noise (from electrocautery, anti-theft systems, etc.). Similarly, an R-wave detection may signal the start of an R-wave in some instances and, in other instances, may identify a T-wave, redetection of the same R-wave, or noise as described previously for P-wave detection.
Various techniques have been developed in an attempt to improve the accuracy of the characterization of cardiac events. For example, post-ventricular atrial blanking (“PVAB”) may act as a parallel refractory period for AF detection. Pre-ventricular atrial blanking (“PREVAB”) may improve far-field R-wave discrimination. Morphology discrimination (e.g., characterizing the shape of a waveform) may be used in an attempt to classify a signal after is has been detected.
The use of these techniques, however, may not guarantee that a stimulation device will provide an accurate indication of all cardiac events. Accordingly a need exists for more effective techniques for identifying cardiac activity.